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Biomedical subjects

S Rosell

Publications and source records attributed to S Rosell.

At least 91 records · Page 5Linked to original sources
PubMed1977

Actions of neurotensin and (Gln4)-neurotensin on isolated tissues.

The actions of neurotensin and (Gln4)-neurotensin have been investigated on a number of isolated tissues. They were ineffective in contracting the guinea pig vas deferens, the rabbit aortic strip or the frog rectus abdominis muscle in concentrations up to 0.24 micron. Neurotensin and (Gln4)-neurotensin relaxed the rat duodenum at fairly high concentrations (24 nM). The guinea pig ileum contracted in response to increasing doses, although the maximum response were only one half that caused by histamine. Tachyphylaxis was observed at dose intervals of less than 12 minutes, but this tachyphylaxis did not inhibit responses to acetylcholine, histamine, 5-HT or to DMPP, suggesting that the neurotensins may act at specific receptor sites. They contracted the rat fundus strip at concentrations of 0.24 nM and higher. The neurotensins and 5-HT were approximately equipotent on this tissue, although the maximum responses was about 80% of that to 5-HT. The contractions of the rat fundus strip could not be blocked by atropine, hexamethonium, methysergide, morphine or by 7-OH-THC. These data indicate that neurotensin and (Gln4)-neurotensin are equipotent as far as smooth muscle stimulating activity is concerned. Of those organs tested, the rat fundus strip seems to be the most suitable one for studies concerning structure-activity relationships.

Acetylcholine↗
PubMed1977

Inhibition of gastric and intestinal motor activity in dogs by (Gln4) neurotensin.

The action of (Gln4)-neurotensin was studied on the spontaneous motor activity in isolated canine fundic, antral and intestinal pouches. All pouches had been prepared more than 6 months prior to the experiments. Spontaneous motor activity was recorded for at least 1 h before the Gln4)-neurotensin was infused i.v. for 30 min in doses ranging between 6.3 and 100 ng X kg-1 X min-1. In the vagally denervated fundic pouches (Gln4)-neurotensin inhibted motor activity in doses above 25 ng X kg-1 X min-1. The vagally innervated antral pouches were more sentitive than the vagally denervated fundic pouches to the action of (Gln4)-neurotensin. Thus motor inhibition was induced by doses as low as 6.3 ng X kg-1 X min-1. The effect of (Gln4)-neurotensin on motor activity in intestinal pouches was inconsistent. Inhibition was seen in 1 out of 7 expts. The present results show that the gastric motor activity is the most sensitive function to (Gln4)-neurotensin so far studied.

Animals↗
PubMed1976

The role of neuronal uptake at alpha- and beta-adrenoceptor sites in subcutaneous adipose tissue.

Intravascular noradrenaline infusion may cause vasodilatation or vasoconstriction in subcutaneous adipose tissue, whereas sympathetic nerve activity causes vasoconstriction only. This discrepancy may be due to a differential distribution of alpha- and beta-adrenoceptors in relation to adrenergic nerve terminals in the adipose tissue vessels. In order to test this hypothesis the extent of prejunctional supersensitivity to noradrenaline was studied after blockade the neuronal uptake of noradrenaline with cocaine. In the autoperfused, isolated inguinal canine adipose tissue pretreatment with coacine (200-600 mug close i.a.) increased lipolysis following sympathetic nerve stimulation or close i.a. injection of noradrenaline. Cocaine also potentiated the vasoconstriction induced by nerve stimulation (1-3 Hz) or intraarterial noradrenaline (0.2-2 nmoles) as well as the vasodilatation induced by sympathetic nerve stimulation (1-3 Hz) after alpha-receptor blockade. However, the vasodilatation following close i.a. injection of noradrenaline after alpha-receptor blockade was not changed by cocaine. The results indicate that the functionally important vascular alpha-adrenoceptors in adipose tissue are in close contact with adrenergic nerve terminals, whereas most vascular beta-adrenoceptors seem to be unrelated to the nerve terminals. Thus, the alpha-adrenoceptors in the adipose tissue vessels may be classified as innervated receptors, in contrast to the vascular beta-adrenoceptors which may be more acessible to circulating catecholamines and may be classified as humoral receptors. Furthermore at least some of the beta-receptors on the adipocytes seem to be located close to sympathetic nerve terminals.

Adipose Tissue↗
PubMed1976

Cardiovascular and metabolic actions of neurotensin and (Gln4)-Neurotensin.

The actions of the tridecapeptides neurotensin and (Gln4)-neurotensin have been studied on the heart and on the blood flow in subcutaneous adipose tissue, skin and small intestine of anesthetized dogs. In addition, their possible actions have been investigated on blood glucose concentration and lipolysis in subcutaneous adipose tissue. The two peptides were found to be approximately equipotent. Intravenous infusion of 20-120 ng X kg-1 X min-1 produced slight hypotension, an initial vasodilatation in the small intestine and a delayed vasoconstriction in denervated subcutaneous adipose tissue and to a lesser extent in the skin and small intestine. At this infusion rate, neurotensin and (Gln4)-neurotensin did not elicit vasodilatation in the skin or adipose tissue and had no effect on heart rate. The delayed vasoconstriction in adipose tissue was not inhibited by local alpha-receptor blockade. Both neurotensin and (Gln4)-neurotensin increased glucose concentration in the upper dose range. No effects on lipolysis were observed, either in vivo or in vitro. These experiments show that neurotensin and (Gln4)-neurotensin have both vasodilator and vasoconstrictor actions in the peripheral vasculature but seem to be without cardiac actions. They also increase blood glucose concentration. It remains to be shown whether these actions are direct or whether some are indirectly mediated.

Adipose Tissue↗